Evidence mapPaperPMID 40897883Full record

ArticlePediatric research2026

Bronchopulmonary dysplasia induced by hyperoxia attenuated by A GLP-1 analog, Liraglutide, by regulating the ACE-2/Ang(1-7)/Mas receptor pathway.

Binglong Huang, Han Luo, Rou Yi Chen, Yeshan Li, Min Xiang, Dang Ao, Shaozhu Lin, Ling Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Binglong Huang *Department of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Han Luo *Department of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Rou Yi ChenDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Yeshan LiDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Min XiangDepartment of orthopaedics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Dang AoDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.
Shaozhu LinDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China. bestlsz@163.com.
Ling LiuDepartment of Pediatrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China. liul37@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucagon-like peptide-1 (GLP-1) shows promise for treating hyperoxia-induced bronchopulmonary dysplasia (BPD), but its mechanisms remain unclear. This study investigated the effects and potential mechanisms of GLP-1 using a hyperoxia-induced neonatal BPD mouse model.

methodsSprague-Dawley (SD) newborn rats were randomly assigned to four groups: control, hyperoxia, hyperoxia+Liraglutide, and hyperoxia+Liraglutide+A779. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected at 3, 7, and 14 days post-exposure to air or hyperoxia. Hyperoxia-induced effects on lung development were assessed using haematoxylin and eosin staining. IL-6, TNF-α, and IL-1β levels in BALF were measured by ELISA. Expression of the ACE/AngII/AT1R and ACE-2/Ang(1-7)/Mas axes was analysed via reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western blotting, and immunohistochemistry.

resultsHyperoxia-induced BPD rats exhibited abnormal alveolar structure, characterized by simplified architecture, thickened septa, and a dysregulated renin-angiotensin system (RAS). Liraglutide significantly reduced hyperoxia-induced levels of IL-1β, TNF-α, and IL-6 in BALF and improved alveolar architecture. Moreover, when comparing the BPD group with the BPD+Lira+A779 group, the BPD+Lira group showed a notable decrease in relative mRNA expression of ACE, AngII, and AT1R (P < 0.05), while mRNA levels of ACE-2 and Ang1 increased significantly (P < 0.05). Consistent with RT-PCR findings, western blot analysis demonstrated that, in the BPD+Lira group, protein levels of ACE and AngII in the lung tissue of neonatal rats significantly lower in the BPD + Liraglutide group at postnatal days 3, 7, and 14 compared to both the BPD and BPD+Liraglutide+A779 groups. Conversely, ACE-2 and Ang(1-7) protein concentrations were markedly elevated. These results suggested that liraglutide may protect against hyperoxia-induced neonatal BPD by suppressing the ACE/AngII/AT1R axis and activating ACE-2/Ang(1-7)/Mas axis, an effect antagonized by A779.

conclusionsThese findings elucidated a mechanism whereby GLP-1 mitigated hyperoxia-induced BPD through inhibition of the ACE/AngII/AT1R pathway and activation of the ACE-2/Ang(1-7)/Mas axis. IMPACT: Liraglutide is capable to protect against hyperoxia-induced neonatal BPD in vitro. Liraglutide mitigated hyperoxia-induced BPD through inhibition of ACE/AngII/AT1R and activation of the ACE-2/Ang(1-7)/Mas axis. The ACE/AngII/AT1R and ACE-2/Ang(1-7)/Mas pathways could be one of those novel mechanisms for treating BPD.

Indexed as

Angiotensin IBronchopulmonary DysplasiaGlucagon-Like Peptide 1HyperoxiaLiraglutidePeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene ProteinsAngiotensin-Converting Enzyme 2AnimalsAnimals, NewbornBronchoalveolar Lavage FluidDisease Models, AnimalLungProto-Oncogene MasRatsAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Glucagon-Like Peptide 1LiraglutidePeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene Proteins

Identifiers

PMID40897883

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.